Research progress of immunometabolic mechanism for GLP-1 to modulate T cell dysfunction in sepsis
10.11855/j.issn.0577-7402.1112.2024.0813
- VernacularTitle:GLP-1调控脓毒症T淋巴细胞功能障碍的免疫代谢机制研究进展
- Author:
Hong-Sheng LIU
1
;
Qing-Hong ZHANG
Author Information
1. 解放军总医院第四医学中心急诊医学科,北京 100048
- Keywords:
glucagon-like peptide-1;
T cell dysfunction;
sepsis;
immunometabolism
- From:
Medical Journal of Chinese People's Liberation Army
2025;50(4):483-489
- CountryChina
- Language:Chinese
-
Abstract:
Persistent inflammation,immuno-suppression and catabolism syndrome(PICS)occurs at the later stage of sepsis,characterized by T cell dysfunction with severe poor outcome.Recent studies found that T cell function be largely affected by its metabolic status.In sepsis,a variety of signaling molecules,including the nutrients,could trigger T cell to undergo metabolic reprogramming that from oxidative phosphorylation to aerobic glycolysis via phosphatidylinositol 3-kinase(PI3K)-serine/threonine kinases(Akt)-mammalian target of rapamycin(mTOR)pathway,leading to severe alterations of its immune phenotype.Glucagon-like peptide-1(GLP-1)is a kind of incretin hormone that could regulate nutrients and energy metabolism in the body.It can reduce blood glucose level,suppress the immune and inflammatory responses.Plasma GLP-1 levels were rapidly elevated in sepsis and correlated closely with the outcome in critical care.GLP-1 receptor(GLP-1R)agonist could block the glycolysis of T cells,reduce glucose transporter type 1 mRNA expression,and inhibit T cell proliferation.Therefore,the elevated GLP-1 level may represent the metabolic switch toward"aerobic glycolysis",reflecting the pathological status of PICS.Here,the review elucidates the regulation of GLP-1 on the immune function and metabolic reprogramming of T cells and provides strategies for the prevention and treatment of T cell immune dysfunction in sepsis via GLP-1 receptor.
